Functional interaction between PARP‐1 and PARP‐2 in chromosome stability and embryonic development in mouse

By J. Ménissier de Murcia, M. Ricoul, L. Tartier, C. Niedergang, Aline Huber, F. Dantzer, V. Schreiber, J. Amé, A. Dierich, M. Lemeur and 3 more. EMBO Journal, 2003

638 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Plant Science

View Paper: https://www.semanticscholar.org/paper/a799fb306055be40fb490d1cac45c17cb2b7dbf9

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Citations in the corpus

PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination (2009, background): “Embryonic knockout of either PARP1 or PARP2 is well tolerated; however, double knockout is embryonic lethal (Menissier de Murcia et al, 2003) suggesting that PARP1 and PARP2 can compensate for some of each other’s functions.”
Laying a trap to kill cancer cells: PARP inhibitors and their mechanisms of action (2016, background): “In mice, the single knockouts of PARP1 or PARP2 are viable, whereas the double knockout of PARP1 and PARP2 is lethal, and double knockout cells exhibit genomic instability (20).”
Repair Pathway Choices and Consequences at the Double-Strand Break (2015, positive): “Indeed, parp1−/− parp2−/− mice display embryonic lethality showing that these proteins have overlapping and nonredundant functions in the maintenance of genomic stability [81].”
Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway. (2008, background): “Importantly, PARP-2, a member of poly-ADP ribose polymerase family (Menissier de Murcia et al., 2003), and Bmf, a member of the Bcl-2 family, is also required for necroptosis induced by either zVAD.fmk or TNFa (Figures 6B and 6C).”
On PAR with PARP: cellular stress signaling through poly(ADP-ribose) and PARP-1. (2012, background): “For example, PARP-1 and PARP-2 can heterodimerize and ADP-ribosylate each other, which may play a role in mediating efficient base excision DNA repair (Schreiber et al. 2002; Menissier de Murcia et al. 2003).”
Poly(ADP-ribose): novel functions for an old molecule (2006, background): “The inactivation of its gene in mice showed that PARP-2 is required for the maintenance of genomic stability and for the efficient repair of single-stranded DNA lesion”
PARP inhibition: PARP1 and beyond (2010, background): “Mice can survive in the absence of Parp1 or Parp2 , for example, but not when both are delete”
The expanding field of poly(ADP-ribosyl)ation reactions. ‘Protein Modifications: Beyond the Usual Suspects' Review Series (2008, background): “Double-knockout mice have also underscored the possible partial redundancy between some parp family members, such as parp1 and parp2, or tankyrase 1 and tankyrase 2 (chiang et al, 2008; Menissier de Murcia et al, 2003) .”
The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings (2011, background): “The most evident role of PARP-2 in suppressing the formation of spontaneous toxic lesions is the embryonic lethal phenotype observed in PARP-1/PARP-2 double knockout mice (Menissier de Murcia et al., 2003), strongly suggesting a role for PARP-2 in some form of DNA repair.”
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase (2005, result): “Depletion of PARP1 and PARP2 resulted in lower clonogenic survival, in agreement with the embryonic lethal phenotype of PARP1 and PARP2 double knockout mic”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “…Single-knockout mice for PARP-1 or PARP-2 are viable, although they display increased genomic instability and hypersensitivity to DNAdamaging agents, while the double knockout is early embryonic-lethal (Wang et al. 1995; de Murcia et al. 1997; Masutani et al. 1999; Menissier de Murcia et al. 2003).”